Animals in the wild periodically go through phases of feast and famine as resources naturally fluctuate and C. elegans have evolved exceptional survival mechanisms when food sources are scarce. Here, we demonstrate that acute adult starvation of C. elegans induces the depletion of somatic fat but these animals retain their germline fat stores. SKN-1 is an established regulator of cellular and organismal stress responses. Recently, we have reported that SKN-1 is a critical mediator of metabolic adaptation and here we define an unprecedented role for SKN-1 in the depletion of somatic fat phenotype. Notably, skn-1 gain-of-function mutant animals, which behave as if they are being starved despite eating ad libitum, mobilize their somatic fat, but only late in their reproductive period. The rapid utilization of somatic fat phenotype is a cell non-autonomous organismal response to ensure reproductive success and we have identified a specific eicosanoid signaling pathway that is responsible for this phenotype. Mechanistically, we have found that vitellogenins are essential for lipid mobilization and this phenotype is intimately tied to available nutrients as the lipid depletion phenotype is influenced by diet and can be suppressed with supplemented dietary carbohydrates. Our results describe a novel mechanism to mobilize nutrient stores, which maximizes the fitness for an organism continually challenged by highly variable food availability.
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